Publications by authors named "Jae-We Cho"

42 Publications

Differential expression of cyclin D1, Ki‑67, pRb, and p53 in psoriatic skin lesions and normal skin.

Mol Med Rep 2018 Jan 8;17(1):735-742. Epub 2017 Nov 8.

Department of Dermatology, Keimyung University School of Medicine, Jung‑Gu, Daegu 41931, Republic of Korea.

Psoriasis is a hyperproliferative inflammatory skin disease; therefore, it is highly likely that psoriatic skin lesions may transform into malignancies. However, malignant transformation is not common. We performed immunohistochemical studies using anti‑cyclin D1, anti‑cyclin E, anti‑pRb, anti‑p53, anti‑p16INK4a, and anti‑Ki‑67 antibodies in normal skin, psoriatic epidermal tissue, and squamous cell carcinoma (SCC) tissue. Furthermore, western blot analysis and immunohistochemical staining were performed to ascertain differences in cyclin D1, cyclin E, pRb, and Ki‑67 expression before and after treatment for psoriasis. Cyclin D1 expression was higher in chronic psoriatic lesions than that in normal epidermis. Psoriasis lesions showed a strong intensity of positive nuclear staining for cyclin D1 among several normally stained nuclei in the basal layer. Cyclin E expression in psoriasis was stronger in the granular and spinous layer than in the normal epidermis. Expression levels of pRb and p53 were found to be higher in the psoriasis group compared with the normal epidermis. Total basal layer cell counts for p53WT expression were found to be significantly higher in the psoriasis group compared with the normal group. However, p16 expression was very weak in the normal and psoriasis groups compared with that in the SCC group. Ki‑67 immunoreactivity was significantly higher in psoriasis compared with normal epidermis and was similar with that in the SCC group. According to immunohistochemistry and immunoblot analysis, the expression levels of cyclin D1, cyclin E, pRb, and Ki‑67 in psoriasis lesions decreased after treatment and were similar with those in the normal group. Thus, increased expression of cyclin D1 and cyclin E may be involved in cell cycle progression in psoriatic epidermis, and pRb and p53 may play important roles in the prevention of malignant transformation under the hyperproliferative state in psoriasis.
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http://dx.doi.org/10.3892/mmr.2017.8015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5780150PMC
January 2018

The Clinical Profile of Patients with Psoriasis in Korea: A Nationwide Cross-Sectional Study (EPI-PSODE).

Ann Dermatol 2017 Aug 21;29(4):462-470. Epub 2017 Jun 21.

Department of Dermatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.

Background: Psoriasis is an immune-mediated, chronic inflammatory disease affecting multiple aspects of patients' lives. Its epidemiology varies regionally; however, nationwide epidemiologic data on psoriasis depicting profile of Korean patients has not been available to date.

Objective: To understand nationwide epidemiologic characteristics and clinical features of adult patients with psoriasis visited university hospitals in Korea.

Methods: This multicenter, non-interventional, cross-sectional study recruited 1,278 adult patients with psoriasis across 25 centers in Korea in 2013. Various clinical data including PASI, BSA, DLQI, SF-36 and PASE were collected.

Results: A total of 1,260 patients completed the study (male:female=1.47:1). The mean age was 47.0 years with a distribution mostly in the 50s (24.9%). Early onset (<40 years) of psoriasis accounted for 53.9% of patients. The mean disease duration was 109.2 months; mean body mass index was 23.9 kg/m; and 12.7% of patients had a family history of psoriasis. Plaque and guttate types of psoriasis accounted for 85.8% and 8.4%, respectively. Patients with PASI ≥10 accounted for 24.9%; patients with body surface area ≥10 were 45.9%. Patients with DLQI ≥6 accounted for 78.8%. Between PASI <10 and PASI ≥10 groups, significant difference was noted in age at diagnosis, disease duration, blood pressure, waist circumference of female, and treatment experiences with phototherapy, systemic agents, and biologics.

Conclusion: This was the first nationwide epidemiologic study of patients with psoriasis in Korea and provides an overview of the epidemiologic characteristics and clinical profiles of this patient population.
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http://dx.doi.org/10.5021/ad.2017.29.4.462DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5500712PMC
August 2017

Introduction of the Reliable Estimation of Atopic Dermatitis in ChildHood: Novel, Diagnostic Criteria for Childhood Atopic Dermatitis.

Allergy Asthma Immunol Res 2016 May;8(3):230-8

Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea.

Purpose: Questionnaire-based diagnostic criteria for atopic dermatitis (AD) have been proposed to detect the major group of AD with flexural dermatitis. We aimed to develop novel, questionnaire-based diagnostic criteria for childhood AD, which can detect more comprehensive AD including non-flexural type.

Methods: The draft version of questionnaire to detect childhood AD was prepared to be used for preliminary hospital- (n=1,756) and community-based (n=1,320) surveys. From analysis, the Reliable Estimation of Atopic dermatitis of ChildHood (REACH) was derived and verified in derivation (n=1,129) and validation (n=1,191) sets by community-based surveys.

Results: The REACH consists of 11 questions including 2 major and 9 minor criteria. AD is diagnosed as the major group of 'eczema on the antecubital or popliteal fossa' to fulfill the 2 major criteria (2M), and the minor group of 'eczema on the non-antecubital or popliteal fossa' to fulfill the 1 major plus 4 or more minor criteria (1M+4m). In the validation set, the overall 1-year AD prevalence by the REACH was estimated as 12.3% (95% CI, 10.5%-14.2%), and the REACH showed a sensitivity of 75.2%, a specificity of 96.1%, and an error rate of 6.4%. The REACH demonstrated better diagnostic performance than the ISAAC in terms of the number of misclassification (10.0%).

Conclusions: We propose the REACH as new full, questionnaire-based diagnostic criteria for childhood AD in epidemiological surveys. Further studies are warranted to validate the REACH in different populations or countries in the context of large-scale, epidemiological surveys.
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http://dx.doi.org/10.4168/aair.2016.8.3.230DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773211PMC
May 2016

A Family-Engaged Educational Program for Atopic Dermatitis: A Seven-Year, Multicenter Experience in Daegu-Gyeongbuk, South Korea.

Ann Dermatol 2015 Aug 29;27(4):383-8. Epub 2015 Jul 29.

Department of Dermatology, Kyungpook National University School of Medicine, Daegu, Korea.

Background: It is important to educate families of pediatric patients with atopic dermatitis (AD) so that they have a correct understanding of AD.

Objective: The purpose of this study is to introduce, evaluate, and improve our family-engaged educational program.

Methods: Children suffering from AD and their families have participated in a half-day educational program called "AD school" with catchy slogans such as "Enjoy with AD Families!" every year since 2005. Educational lectures were conducted for parents. For children with AD, various entertaining programs were provided. A feedback survey about AD school was administered for the purpose of evaluation.

Results: A total of 827 people (376 patients and 451 family members) participated in this program over 7 years. On-site surveys showed a positive response (i.e., "excellent" or "good") for the prick test (95.1%), emollient education (78.4%), educational lecture (97.0%), drawing contest and games (90.2%), and recreation (magic show; 99.0%) respectively. Telephone surveys one year later also elicited a positive response.

Conclusion: We herein introduce the experience of a half-day, family-engaged educational program for AD. Family-engaged education programs for AD such as this AD school encourage and validate family participation in the treatment of their children's AD.
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http://dx.doi.org/10.5021/ad.2015.27.4.383DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4530146PMC
August 2015

Weber-Cockayne Type Epidermolysis Bullosa Simplex Resulting from a Novel Mutation (c. 608T>C) in the Keratin 5 Gene.

Ann Dermatol 2014 Dec 26;26(6):739-42. Epub 2014 Nov 26.

Department of Dermatology, Keimyung University School of Medicine, Daegu, Korea.

Epidermolysis bullosa simplex (EBS), an inherited genetic disorder, is most often caused by a dominant-negative mutation in either the keratin 5 (KRT5) or the keratin 14 (KRT14) gene. These keratin mutants result in a weakened cytoskeleton and cause extensive cytolysis. It is important to analyze the KRT5 or KRT14 genes of the patient and their family members by mutational analysis in order to identify genetic defects as well as the need for genetic counseling. In this study, we present a 5-year-old Korean boy who had been developing blisters and erosions on the palms of his hands and soles of his feet since infancy. In addition, while his younger sister and father showed similar clinical manifestation, his mother did not. The patient was diagnosed with EBS based on clinical manifestation, which is characterized by the presence of blisters restricted to the palms and soles, histological findings, and mutational analysis. Mutational analysis of the patient's DNA revealed a thymine-to-cytosine transition at codon 608 in the KRT-5 gene, resulting in a leucine-to-proline substitution in the keratin 5 protein. The same mutation was identified in the paternal, but not maternal, DNA. Here, we report a case of Weber-Cockayne type EBS with vesicles and bullae restricted to the palms and soles with a novel, paternally inherited mutation in KRT5 gene (exon2, c.608T>C).
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http://dx.doi.org/10.5021/ad.2014.26.6.739DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4252672PMC
December 2014

Prevention of thyroidectomy scars in Korean patients using a new combination of intralesional injection of low-dose steroid and pulsed dye laser starting within 4 weeks of suture removal.

Dermatol Surg 2014 May 9;40(5):562-8. Epub 2014 Apr 9.

Department of Dermatology, School of Medicine, Keimyung University, Daegu, South Korea.

Background: Regulation of inflammation during the wound healing process reduces scar formation at the injury site.

Objective: To evaluate the effect of intralesional injection of low-dose steroid with pulsed dye laser on healing of early postoperative thyroidectomy scars.

Materials And Methods: Twenty Korean women with thyroidectomy scars were enrolled. All were treated with an intralesional injection of low-dose steroid (2 mg/mL) and 595-nm pulsed dye laser starting within 4 weeks of suture removal. The Vancouver Scar Scale (VSS), Global Assessment Score (GAS), and Patient Satisfaction Score were used in this evaluation.

Results: Average VSS scores were significantly lower after treatment. The GAS also indicated better cosmetic outcomes after steroid injection in the laser treatment group than after laser treatment only.

Conclusion: Early postoperative intralesional injection of low-dose steroid and pulsed dye laser treatment is effective and safe.
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http://dx.doi.org/10.1111/dsu.12472DOI Listing
May 2014

Recombinant growth factor mixtures induce cell cycle progression and the upregulation of type I collagen in human skin fibroblasts, resulting in the acceleration of wound healing processes.

Int J Mol Med 2014 May 14;33(5):1147-52. Epub 2014 Mar 14.

Department of Dermatology, Chung-Ang University College of Medicine, Seoul, Republic of Korea.

Application of growth factor mixtures has been used for wound healing and anti-wrinkles agents. The aim of this study was to evaluate the effect of recombinant growth factor mixtures (RGFM) on the expression of cell cycle regulatory proteins, type I collagen, and wound healing processes of acute animal wound models. The results showed that RGFM induced increased rates of cell proliferation and cell migration of human skin fibroblasts (HSF). In addition, expression of cyclin D1, cyclin E, cyclin-dependent kinase (Cdk)4, and Cdk2 proteins was markedly increased with a growth factor mixtures treatment in fibroblasts. Expression of type I collagen was also increased in growth factor mixtures-treated HSF. Moreover, growth factor mixtures-induced the upregulation of type I collagen was associated with the activation of Smad2/3. In the animal model, RGFM-treated mice showed accelerated wound closure, with the closure rate increasing as early as on day 7, as well as re-epithelization and reduced inflammatory cell infiltration than phosphate-buffered saline (PBS)-treated mice. In conclusion, the results indicated that RGFM has the potential to accelerate wound healing through the upregulation of type I collagen, which is partly mediated by activation of Smad2/3-dependent signaling pathway as well as cell cycle progression in HSF. The topical application of growth factor mixtures to acute and chronic skin wound may accelerate the epithelization process through these molecular mechanisms.
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http://dx.doi.org/10.3892/ijmm.2014.1698DOI Listing
May 2014

Safety evaluation of topical valproate application.

Toxicol Res 2013 Jun;29(2):87-90

Department of Dermatology, Chung-Ang University College of Medicine, Seoul, Korea.

The potential role of topical valproate (VPA) in hair regrowth has been recently suggested. However, safety reports of VPA as a topical formulation are lacking. Therefore, in the present study, we investigated whether VPA causes skin irritation in humans. We first performed a cell viability test and showed that VPA did not exhibit toxicity toward HaCaT keratinocytes, fibroblasts, and RBL-3H mast cells. We then performed clinical patch test and skin irritation test through transdermal drug delivery with the help of microneedle rollers. No significant findings were obtained in the clinical patch test. In the skin irritation test, only 1 patient showed erythema at 1 hr, but the irritation reaction faded away within a few hours. Erythema and edema were not observed at 24 hr. We concluded that VPA has minimal potential to elicit skin irritation. Therefore, we consider that VPA can safely be applied to human skin.
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http://dx.doi.org/10.5487/TR.2013.29.2.087DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834454PMC
June 2013

Photodynamic therapy combined with cryotherapy for the treatment of nodular basal cell carcinoma.

Oncol Lett 2013 Oct 31;6(4):939-941. Epub 2013 Jul 31.

Department of Dermatology, Keimyung University School of Medicine, Dongsan-dong, Jung-gu, Daegu 700-712, Republic of Korea.

Carbon dioxide (CO) laser ablation in combination with photodynamic therapy (PDT) has previously been successfully used to treat superficial basal cell carcinoma (BCC). However, the efficacy of this treatment modality is limited in the treatment of deeper lesions and the more aggressive subtypes of BCC. In order to improve the outcome of PDT, 8 BCC lesions of variable depths (4 lesions ≤2 mm and 4 lesions >2 mm) and subtypes (1 superficial, 6 nodular and 1 infiltrative) were treated with CO laser ablation in combination with PDT, followed by modified cryotherapy. The mean number of treatment sessions was 1.5 and the follow-up period was 22 months. All of the patients demonstrated a complete response and no recurrence of disease, while the majority of patients were satisfied with the cosmetic results upon follow-up examination. The combination therapy of CO laser ablation with PDT followed by modified cryotherapy demonstrated a good efficacy and satisfactory cosmetic outcomes in the treatment of nodular BCC.
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http://dx.doi.org/10.3892/ol.2013.1504DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3796394PMC
October 2013

Clinical improvement of striae distensae in Korean patients using a combination of fractionated microneedle radiofrequency and fractional carbon dioxide laser.

Dermatol Surg 2013 Oct 29;39(10):1452-8. Epub 2013 Jul 29.

Department of Dermatology, Keimyung University School of Medicine, Daegu, South Korea.

Background: Striae distensae are dermal scars with flattening and atrophy of the epidermis.

Objective: To evaluate the efficacy and safety of combination therapy with fractionated microneedle radiofrequency (RF) and fractional carbon dioxide (CO2) laser in the treatment of striae distensae.

Materials And Methods: Thirty patients (30 female; mean age 33, range 21-51, Fitzpatrick skin type IV) with moderate to severe striae distensae were enrolled in this study. Patients were divided into three groups: fractional CO2 laser only (n = 10), microneedle RF only (n = 10), and combination (n = 10).

Results: Improvement was evaluated using a visual analogue scale (range 1-4). Mean clinical improvement score of the dermatologist was 2.2 in the fractional CO2 laser-treated group, 1.8 in the microneedle RF-treated group, and 3.4 in the combination group. Through skin biopsy, we observed thickened epidermis and a clear increase in the number of collagen fibers in the microneedle RF- and fractional CO2 combination-treated sites. Consistent with these results, greater expression of transforming growth factor-β1 and stratifin was observed in treated sites.

Conclusion: Combination therapy of fractionated microneedle RF and fractional CO2 laser is a safe treatment protocol with a positive therapeutic effect on striae distensae.
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http://dx.doi.org/10.1111/dsu.12268DOI Listing
October 2013

Downregulation of type I collagen expression in silibinin-treated human skin fibroblasts by blocking the activation of Smad2/3-dependent signaling pathways: potential therapeutic use in the chemoprevention of keloids.

Int J Mol Med 2013 May 14;31(5):1148-52. Epub 2013 Mar 14.

Department of Dermatology, Keimyung University School of Medicine, Jung-Gu, Daegu 700-712, Republic of Korea.

The inhibition of the Smad2/3 pathway is a key step involved in the downregulation of type I collagen synthesis, thus preventing keloid formation in tissue. In this study, we investigated the effect of silibinin on the proliferation of human skin fibroblasts (HSFs), as well as its effect on the expression of type I collagen, matrix metalloproteinase (MMP)-1, Smad2 and Smad3. Our results showed that the proliferation rates of the fibroblasts were not markedly decreased in a dose- and time-dependent manner following treatment with silibinin. Even though silibinin did not exert any cytotoxic effects on HSFs, the expression of type I collagen was markedly decreased in a dose- and time-dependent manner in the silibinin-treated HSFs. Consistent with this finding, the decreased promoter activity of type I collagen was observed in the HSFs following treatment with silibinin. The MMP-1 and MMP-2 expression levels were increased in the silibinin-treated HSFs. Moreover, the silibinin-induced downregulation of type I collagen was associated with the inhibition of Smad2/3 activation in the transforming growth factor‑β1 (TGF-β1)-treated HSFs. We further demonstrated that silibinin attenuated the translocation of Smad2 and Smad3 to the nucleus in the TGF-β1-treated HSFs. Taken together, our data indicate that silibinin has the potential to prevent fibrotic skin changes by inducing the downregulation of type I collagen expression; this effect was partly mediated by the inhibition of the Smad2/3-dependent signaling pathway in HSFs.
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http://dx.doi.org/10.3892/ijmm.2013.1303DOI Listing
May 2013

Application of platelet-rich plasma accelerates the wound healing process in acute and chronic ulcers through rapid migration and upregulation of cyclin A and CDK4 in HaCaT cells.

Mol Med Rep 2013 Feb 12;7(2):476-80. Epub 2012 Dec 12.

Department of Dermatology, Keimyung University School of Medicine, Daegu 700-712, Republic of Korea.

Application of autologous platelet-rich plasma (PRP) has been used for chronic wound healing. The aim of this study was to evaluate the effect of PRP on the wound healing processes of both acute and chronic ulcers and the underlying molecular mechanisms involved. We treated 16 patients affected by various acute and chronic ulcers with PRP. We performed molecular studies of cell proliferation, migration assays, immunoblotting and chloramphenicol acetyltransferase (CAT) assays in PRP-treated HaCaT keratinocyte cells. PRP treatment induced increased rates of cell proliferation and cell migration of HaCaT cells. In addition, the expression of cyclin A and cyclin dependent kinase (CDK) 4 proteins was markedly increased with a low concentration (0.5%) of PRP treatment in HaCaT cells. In 11 patients with chronic ulcers, including stasis ulcers, diabetic ulcers, venous leg ulcers, livedoid vasculitis, claw foot and traumatic ulcers, 9 patients showed 90-100% epithelization after 15.18 days. In 5 patients with acute ulcers, such as dehiscence, open wound and burn wound, 80-100% epithelization was achieved between 4 to 20 days. Topical application of PRP to acute and chronic skin ulcers significantly accelerated the epithelization process, likely through upregulation of the cell cycle regulatory proteins cyclin A and CDK4.
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http://dx.doi.org/10.3892/mmr.2012.1230DOI Listing
February 2013

Pityriasis versicolor on penile shaft in a renal transplant recipient.

Ann Dermatol 2012 Aug 25;24(3):345-7. Epub 2012 Jul 25.

Department of Dermatology, Keimyung University School of Medicine, Daegu, Korea.

Pityriasis versicolor is a superficial infection of the stratum corneum, which is caused by the Malassezia species. Tge Malassezia species consist of 12 subspecies, including M. furfur, M. pachydermatis, M. symphodialis and M. globasa. The Malassezia species are classified as a normal flora, particularly in the sebum rich areas of the skin, and they convert from saprophytic yeast to parasitic mycelial morpholgic form to cause clinical disease. But majorities of their distributions are in the upper back, the neck, the thighs, and the forearm, and not in the penis. It is well known that the renal transplant patients, who take immunosuppressive agents, have impairment in the protective cell mediated immunity. Thus, they are more susceptible to infectious diseases, such as a fungal infection. Therefore, clinical manifestations show higher incidence of disease, but they mostly occur in an expected distribution. We here report a case of pityriasis versicolor in a renal transplant recipient on penile shaft, which is an unusual area.
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http://dx.doi.org/10.5021/ad.2012.24.3.345DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412245PMC
August 2012

Primary Extramammary Paget's Disease Combined with Bowen's Disease in Vulva.

Ann Dermatol 2011 Oct 31;23(Suppl 2):S222-5. Epub 2011 Oct 31.

Department of Dermatology, Keimyung University School of Medicine, Daegu, Korea.

Extramammary Paget's disease (EMPD) is a uncommon neoplastic condition of apocrine gland-bearing skin and its occurrence in combination with Bowen's disease is very rare. The most common site of involvement is the vulva, although perineal, perianal, scrotal and penile skin may also be affected. EMPD is usually not combined with Bowen's disease. We report an interesting case of EMPD combined with Bowen's disease, which was confirmed by immunohistochemical stain.
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http://dx.doi.org/10.5021/ad.2011.23.S2.S222DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229071PMC
October 2011

Skin Hydration and Collagen Synthesis of AF-343 in HS68 Cell Line and NC/Nga Mice by Filaggrin Expression and Suppression of Matrix Metallopreteinase.

Toxicol Res 2011 Dec;27(4):225-9

Department of Dermatology, School of Medicine, Keimyung University, Daegu 700-712, Korea.

Extract of Taraxacum platycarpum (AF-343) has been reported to have several biological properties such as skin hydration and anti-inflammatory effects. Although clinical evidences of skin hydration and antiinflammatory effect were proven in clinical trial, precise mechanism of skin hydration was not fully understood yet. In this study, we have focused skin hydration mechanism related filaggrin, collagen, and matrix metalloproteinase (MMP) in vitro and animal study. Herein, skin hydration mechanism of AF-343 is due to recovery of filaggrin in mice model and increased production of collagen with suppression of matrix MMP in vitro fibroblast cell line.
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http://dx.doi.org/10.5487/TR.2011.27.4.225DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834392PMC
December 2011

Platelet-rich plasma induces increased expression of G1 cell cycle regulators, type I collagen, and matrix metalloproteinase-1 in human skin fibroblasts.

Int J Mol Med 2012 Jan 30;29(1):32-6. Epub 2011 Sep 30.

Department of Dermatology, Keimyung University School of Medicine, Daegu, Republic of Korea.

Platelet-rich plasma (PRP) is derived from fresh whole blood, which contains a high concentration of platelets. Recently, PRP has been used for skin wound healing and rejuvenation. However, the molecular mechanisms underlying PRP-inducing wound healing processes are still largely unknown. The aim of this study is to evaluate the effect of PRP on the expression of G1 cell cycle regulatory proteins, type I collagen, matrix metalloproteinase-1 (MMP-1), and MMP-2 in human skin fibroblasts (HSF). We performed a cell proliferation and a migration assay, immunoblotting, and a chloramphenicol acetyltransferase (CAT) assay in PRP-treated human skin fibroblasts. PRP treatment induced increased rates of cell proliferation and cell migration. Expression of cyclin A protein was increased by a low concentration (0.5%) of PRP-treated HSF. In addition, expression of Rb, cyclin E, and cyclin-dependent kinase 4 proteins was increased by a high concentration (5%) of PRP-treated HSF. High concentration of PRP induced an up-regulation of type I collagen, MMP-1, and MMP-2 expression in HSF. Taken together, PRP treatment induced an increase in expression of G1 cell cycle regulators, type I collagen and MMP-1, thereby accelerating the wound healing process.
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http://dx.doi.org/10.3892/ijmm.2011.803DOI Listing
January 2012

Proteomic analysis of psoriatic skin tissue for identification of differentially expressed proteins: up-regulation of GSTP1, SFN and PRDX2 in psoriatic skin.

Int J Mol Med 2011 Nov 25;28(5):785-92. Epub 2011 Jul 25.

Medical Proteomics Research Center, KRIBB, Daejeon, Republic of Korea.

Psoriasis is a chronic inflammatory skin disease, characterized by a combination of abnormal proliferation of keratinocytes, immunology and vascular proliferation. Proteomic analyses have revealed some clues regarding the pathogenesis of psoriasis. In the present study, we conducted an investigation of different proteomes of psoriatic lesional skin, and compared them with those of normal and non-lesional psoriatic skin. We performed 2-D gel electrophoresis, liquid chromatography tandem mass spectrometry (LC-MS/MS) analysis and database searches. Expression of proteins were evaluated by immunoblot and immunohistochemistry analyses. Our data showed differential expression of 74 and 145 protein spots in non-lesional and lesional psoriatic skin, respectively. Eleven of 36 proteins, which were identified by LC-MS/MS, were categorized as apoptosis-regulating proteins. Other protein spots were categorized as proteins with involvement in the negative regulation of apoptosis, defense response-related proteins and inflammatory response. Of particular interest, increased expression of glutathione S transferase 1 (GSTP1) and peroxiredoxin 2 (PRDX2), which are involved in the Redox balance system, and SFN, which is involved in the cellular proliferation system, was observed in psoriatic lesional skin. Localization of GSTP1 and SFN was observed above the middle layer of the epidermis in psoriatic skin lesions. Expression of PRDX2 was clearly observed below the middle layer of the epidermis in chronic type psoriatic skin lesions. Taken together, 36 identified proteins were associated with biological regulation, including regulation of cell death, defense response, inflammatory response and reactive oxygen species (ROS) regulation. PRDX2 and GSTP1 may play roles in compensating mechanisms for reduction of ROS stress, and SFN may play roles in prevention of cancer development in proliferating cells through G2/M cell cycle arrest upon accidental DNA damage within psoriatic skin lesions.
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http://dx.doi.org/10.3892/ijmm.2011.757DOI Listing
November 2011

A case of an unusual eccrine poroma on the left forearm area.

Ann Dermatol 2011 May 27;23(2):250-3. Epub 2011 May 27.

Department of Dermatology, School of Medicine, Keimyung University, Daegu, Korea.

A 40-year-old woman presented with an asymptomatic red to brown colored walnut-sized, dome shaped, hemorrhagic, crusted nodule on the left forearm. There was no previous history of trauma to the area. The first impression of this case was a vascular tumor or malignant lesion due to the large size and bleeding tendency. However, the final diagnosis, according to histologic and immunostaining methods, was a benign eccrine poroma that occurred on the left forearm, which is an unusual area for such a lesion. The tumor was excised and no recurrence was noted when she was examined 24 months later.
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http://dx.doi.org/10.5021/ad.2011.23.2.250DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3130877PMC
May 2011

TGF-β1-treated ADSCs-CM promotes expression of type I collagen and MMP-1, migration of human skin fibroblasts, and wound healing in vitro and in vivo.

Int J Mol Med 2010 Dec;26(6):901-6

Department of Dermatology, Keimyung University School of Medicine, 194 DongSan-Dong Jung-Gu, Daegu, Korea.

Conditioned medium from adipose-derived stem cells (ADSCs) stimulates both collagen synthesis and migration of dermal fibroblasts. However, it is still unknown whether conditioned media from tumor growth factor (TGF)-β1-treated ADSCs (TGF-β1-treated ADSCs-CM) induces increased expression of type I collagen, matrix metalloproteinase-1 (MMP-1), and migration as well as cell cycle regulatory proteins in fibroblasts, compared to non-treated ADSCs-CM. Our data showed that TGF-β1-treated ADSCs-CM promoted effectively the proliferation and migration of human skin fibroblasts, compared to non-treated ADSCs-CM. In addition the expression of MMP-1 were markedly increased by treatment of TGF-β1-treated ADSCs-CM in fibroblasts, compared to non-treated ADSCs-CM. Expression of type I collagen protein were slightly increased by treatment of TGF-β1-treated ADSCs-CM in fibroblasts. The expression of cell cycle regulators of G1/S phase transition were not markedly altered by treatment of TGF-β1-treated ADSCs-CM. Finally, artificial wounds were made using a 4-mm punch biopsy in hairless mice and TGF-β1-treated ADSCs-CM were injected into the wound area. The injection of TGF-β1-treated ADSCs-CM promoted the wound healing process in hairless mice. Taken together, our data indicated that TGF-β1-treated ADSCs-CM induced up-regulation of type I collagen and MMP-1, promoted the migration of skin fibroblasts, and thereby promoted the wound healing process in vivo. Our data indicate that TGF-β1-treated ADSCs-CM will be a component for a wound healing accelerating agent.
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http://dx.doi.org/10.3892/ijmm_00000540DOI Listing
December 2010

Down-regulation of IL-6, IL-8, TNF-α and IL-1β by glucosamine in HaCaT cells, but not in the presence of TNF-α

Oncol Lett 2010 Mar 1;1(2):289-292. Epub 2010 Mar 1.

Department of Dermatology, College of Medicine Eulji University, Seoul.

There is considerable evidence that glucosamine exerts an inhibitory effect on inflammatory cytokine expression in cells. Glucosamine has been recommended as a promising anti-inflammatory modulator, which has been applied in clinical trials for attenuation of the inflammatory process. However, it is unknown whether glucosamine reduces the expression of TNF-α-induced inflammatory cytokines in HaCaT cells. The anti-inflammatory effects of curcumin in HaCaT cells have been extensively investigated in several studies. Thus, in this study we investigated the expression of IL-6, IL-8, TNF-α and IL-1β in glucosamine-treated HaCaT cells, and the effects of glucosamine were compared to those of curcumin-treated HaCaT cells. Our data showed that the expression of IL-6, IL-8, TNF-α and IL-1β was decreased by glucosamine treatment in the HaCaT cells. In contrast, the expression of IL-6, IL-8, TNF-α and IL-1β was not attenuated by glucosamine treatment in the TNF-α-treated HaCaT cells. Notably, curcumin induced an increased expression of IL-8 and IL-1β in the HaCaT cells, but not that of IL-6 and TNF-α. On the other hand, curcumin attenuated the expression of IL-6 and IL-8 in the TNF-α-treated HaCaT cells. Our data indicated that glucosamine induced the down-regulation of IL-6, IL-8, TNF-α and IL-1β expression in the HaCaT cells. However, the stimulation of TNF-α abolished the inhibitory effects of glucosamine on the expression of inflammatory cytokines in the HaCaT cells. Thus, even though glucosamine induces the down-regulation of inflammatory cytokines in HaCaT cells, the anti-inflammatory role of glucosamine in TNF-α-mediated inflammatory skin diseases should be investigated.
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http://dx.doi.org/10.3892/ol_00000051DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436374PMC
March 2010

Onion extract and quercetin induce matrix metalloproteinase-1 in vitro and in vivo.

Int J Mol Med 2010 Mar;25(3):347-52

Department of Dermatology, School of Medicine, Daegu 700-712, Korea.

A scar is usually developed by an imbalance of collagen synthesis and degradation. It is believed that the flavonoids (quercetin and kaempferol) in onion extract play a role in reducing scar formation through inhibition of fibroblast activities. Even though several commercial products are composed of onion extract, the precise molecular mechanisms of onion extract in reduction of scar formation in skin are still largely unknown. In this study we investigated the effect both of onion extract and quercetin on the proliferation of fibroblasts, expression of type I collagen and matrix metalloproteinase-1 (MMP-1). Our data show that proliferation rates of fibroblasts were decreased in a dose-dependent manner of the onion extract and quercetin. The expression of type I collagen was not markedly changed by the onion extract and quercetin. Interestingly, the expression of MMP-1 was markedly increased by both onion extract and quercetin in vitro and in vivo. Thus, our data indicate that onion extract and quercetin play a role in the anti-scar effect in skin through up-regulation of MMP-1 expression, implying this agent is a promising material for reducing scar formation.
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March 2010

Type VII collagen gene mutations (c.8569G>T and c.4879G>A) result in the moderately severe phenotype of recessive dystrophic epidermolysis bullosa in a Korean patient.

J Korean Med Sci 2009 Apr 20;24(2):256-61. Epub 2009 Apr 20.

Department of Dermatology, Keimyung University, School of Medicine, Daegu, Korea.

Dystrophic epidermolysis bullosa (DEB) are caused by mutations in the COL7A1 gene, which encodes type VII collagen. Even though more than 500 different COL7A1 mutations have been identified in DEB, it still remains to be under-investigated. To investigate the mutation of COL7A1 in moderately severe phenotype of recessive DEB (RDEB) in a Korean patient, the mutation detection strategy was consisted of polymerase chain reaction (PCR) amplification of genomic DNA, followed by heteroduplex analysis, nucleotide sequencing of the PCR products demonstrating altered mobility. In this study, we found that one mutation (c.8569G>T) was detected within exon 116. The mutation of c.8569G>T in exon 116 changed the GAG (Glu) to TAG, eventually resulted in premature termination of type VII collagen polypeptide. Furthermore the mother did not have the mutation c.8569G>T in exon 116. The other novel mutation (c.4879G>A) was detected within exon 51 of both patient and mother, thereby resulting in changing valine (Val) to isoleucine (Ile) in type VII collagen polypeptide. Taken together, in this study we identified compound heterozygosity for COL7A1 mutations (c.8569G>T and c.4879G>A) in moderately severe RDEB in a Korean patient. We hope that this data contribute to the expanding database on COL7A1 mutations in DEB.
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http://dx.doi.org/10.3346/jkms.2009.24.2.256DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672125PMC
April 2009

Roles of SEA-expressing Staphylococcus aureus, isolated from an atopic dermatitis patient, on expressions of human beta-defensin-2 and inflammatory cytokines in HaCaT cells.

Int J Mol Med 2009 Mar;23(3):331-5

Department of Dermatology, School of Medicine, Keimyung University, Daegu 700-712, South Korea.

Atopic dermatitis (AD) shows an increased susceptibility to Staphylococcus aureus infection partly due to decreased expression of human beta-defensin-2 (HBD-2). Interestingly, it was reported that the nasal carrier S. aureus down-regulates the expression of HBD-2 and -3, thereby the carrier strains of S. aureus retain an advantage to epithelial colonization and infection. In this study, we tried to isolate and characterize S. aureus from an AD patient, with recurrent oozing on his face. We studied the increased expression of inflammatory cytokines, such as IL-1beta, -6, -8, and TNF-alpha in S. aureus treated-HaCaT cells, which are mediated by secreting superantigens (SAgs), structural component, or both. In addition, we investigated whether the SAgs from S. aureus can down-regulate the expression of HBD-2 in HaCaT cells making favorable conditions for colonization on skin. Our data showed that the isolated S. aureus has the exotoxin gene, sea exotoxin. The SEA producing-S. aureus induced the expression of IL-1beta, -6, -8 cytokines, and TNF-alpha in HaCaT cells. The expression of HBD-2 was increased in S. aureus-treated HaCaT cells. Furthermore IL-8 was also induced by the structure component of S. aureus. Taken together, the SEA producing S. aureus induced the up-regulation of pro-inflammatory cytokines as well as HBD-2, thereby resulting in induction of the persistent eczematous skin lesions in AD. Thus, our data may give insight into understanding the pathogenesis by which S. aureus induces and aggravates eczematous skin lesions in AD.
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http://dx.doi.org/10.3892/ijmm_00000135DOI Listing
March 2009

AP-1 transcription factor decoy reduces the TGF-beta1-induced cell growth in scleroderma fibroblasts through inhibition of cyclin E.

Oncol Rep 2008 Mar;19(3):737-41

Department of Dermatology, Keimyung University School of Medicine, Daegu 700-712, Korea.

The transforming growth factor-beta (TGF-beta) signaling pathway plays a key role in the abnormal accumulation of type I and III collagen of scleroderma. Activator protein-1 (AP-1) is a key regulatory protein in TGF-beta1-induced type I collagen synthesis. However, it is largely unknown whether AP-1 is involved in the cell proliferation of fibroblasts in scleroderma. In this study, we investigated the effects of the AP-1 oligo-deoxynucleotide (ODN) decoy on TGF-beta1-induced cell growth in scleroderma fibroblasts. To investigate the inhibition of AP-1 ODN decoy on the growth rates of scleroderma fibroblasts through the regulation of cell cycle regulatory proteins, we transfected the AP-1 ODN decoy on scleroderma fibroblasts and analyzed the cell cycle regulatory proteins by RT-PCR and Western blot analysis. We found that the growth rates of normal fibroblasts and scleroderma fibroblasts showed similar rates. It is noteworthy that the scleroderma fibroblasts grew more rapidly than normal fibroblasts in the presence of TGF-beta1. Moreover, the transfection of AP-1 decoy ODN into scleroderma fibroblasts resulted in the down-regulation of the growth rates by the down-regulation of cyclin E. These results collectively suggest that AP-1 ODN decoy can down-regulate the growth rates of scleroderma fibroblasts, thus implying that AP-1 ODN decoy is a promising therapeutic tool for overcoming scleroderma.
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March 2008

Curcumin attenuates the expression of IL-1beta, IL-6, and TNF-alpha as well as cyclin E in TNF-alpha-treated HaCaT cells; NF-kappaB and MAPKs as potential upstream targets.

Int J Mol Med 2007 Mar;19(3):469-74

Department of Dermatology, School of Medicine, Keimyung University, Daegu 700-712, Korea.

TNF-alpha induces some proinflammatory cytokines including IL-1beta, IL-6, IL-8, and itself by activation of NF-kappaB or MAPKs (p38, JNK, ERK). These cytokines play important roles in various inflammatory skin diseases, such as psoriasis. Recently it was also reported that expression of cyclin E is up-regulated by ERK pathway after TNF-alpha treatment. However, it was unknown whether curcumin, showing inhibitory effects on NF-kappaB and MAPKs, attenuates the expression of TNF-alpha-induced IL-1beta, IL-6, IL-8, and TNF-alpha as well as cyclin E expression in HaCaT cells. In this study, we investigated the inhibitory effect of curcumin on expression of proinflammatory cytokines and cyclin E in TNF-alpha-treated HaCaT cells. We found that curcumin inhibited the expression of TNF-alpha-induced IL-1beta, IL-6, and TNF-alpha, but not IL-8, in TNF-alpha-treated HaCaT cells as well as the TNF-alpha-induced cyclin E expression. In addition, curcumin inhibited the activation of MAPKs (JNK, p38 MAPK, and ERK) and NF-kappaB in TNF-alpha-treated HaCaT cells. Taken together, curcumin exerts anti-inflammatory and growth inhibitory effects in TNF-alpha-treated HaCaT cells through inhibition of NF-kappaB and MAPK pathways.
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March 2007

Modification of gene expression by melatonin in UVB-irradiated HaCaT keratinocyte cell lines using a cDNA microarray.

Oncol Rep 2007 Mar;17(3):573-7

Department of Dermatology, Keimyung University School of Medicine, Daegu 700-712, South Korea.

Excessive ultraviolet B (UVB) irradiation causes apoptotic cell death or induction of tumors in skin. Melatonin is a promising antioxidant and direct radical scavenger. Recently, it was reported that melatonin increases the survival of ultraviolet-B (UVB)-irradiated HaCaT keratinocyte cell lines. However, the precise molecular mechanisms underlying protective effect of melatonin on UVB damage are largely unknown. In this study, to gain more insight into the molecular mechanisms involved in melatonin-induced cell survival on UVB-irradiated HaCaT keratinocytes, we performed cDNA microarray analysis. HaCaT keratinocytes were incubated without or with melatonin at 100 nm for 30 min prior to UVB irradiation at 100 mJ/cm(2), and total RNA was isolated. Our data showed that the expression of apoptosis regulator genes (apoptosis related protein-3, apoptotic chromatin condensation inducer in the nucleus), cancer related genes (tumor suppressor deleted in oral cancer-related 1), cell cycle regulator (cyclin-dependent kinase 2 interacting protein), enzymes (glutathione peroxidase 1, ubiquitin-conjugating enzyme E2M), and signal transducer genes [fibroblast growth factor (acidic) intracellular binding protein, transforming growth factor beta-stimulated protein TSC-22] were decreased by melatonin treatment in the UVB-irradiated HaCaT keratinocyte cell lines, compared to that of UVB-irradiated HaCaT cells without melatonin. Thus, findings of the present study demonstrate that melatonin modulates the expression of apoptosis related genes in UVB-irradiated HaCaT cells, resulting in increasing cell survival, thereby suggesting that melatonin may be used as a promising sunscreen substance to reduce cell death of keratinocytes after excessive UVB irradiation.
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March 2007

Thimerosal induces apoptosis and G2/M phase arrest in human leukemia cells.

Mol Carcinog 2006 Sep;45(9):657-66

Department of Immunology, School of Medicine, Keimyung University, Taegu, South Korea.

Thimerosal is an organomercury compound with sulfhydryl-reactive properties. The ability of thimerosal to act as a sulfhydryl group is related to the presence of mercury. Due to its antibacterial effect, thimerosal is widely used as preservatives and has been reported to cause chemically mediated side effects. In the present study, we showed that the molecular mechanism of thimerosal induced apoptosis in U937 cells. Thimerosal was shown to be responsible for the inhibition of U937 cells growth by inducing apoptosis. Treatment with 2.5-5 microM thimerosal but not thiosalicylic acid (structural analog of thimerosal devoid of mercury) for 12 h produced apoptosis, G(2)/M phase arrest, and DNA fragmentation in a dose-dependent manner. Treatment with caspase inhibitor significantly reduced thimerosal-induced caspase 3 activation. In addition, thimerosal-induced apoptosis was attenuated by antioxidant Mn (III) meso-tetrakis (4-benzoic acid) porphyrin (Mn-TBAP). These data indicate that the cytotoxic effect of thimerosal on U937 cells is attributable to the induced apoptosis and that thimerosal-induced apoptosis is mediated by reactive oxygen species generation and caspase-3 activation.
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http://dx.doi.org/10.1002/mc.20202DOI Listing
September 2006

Curcumin inhibits the expression of COX-2 in UVB-irradiated human keratinocytes (HaCaT) by inhibiting activation of AP-1: p38 MAP kinase and JNK as potential upstream targets.

Exp Mol Med 2005 Jun;37(3):186-92

Department of Dermatology, Keimyung University, School of Medicine, 194 DongSan-dong Jung-gu, Daegu 700-712, Korea.

Ultraviolet B (UVB) irradiation of skin induces an acute inflammation. Cyclooxygenase-2 (COX-2) protein plays key roles in acute inflammation in UVB-irradiated keratinocyte cell line HaCaT. Recently, curcumin has been regarded as a promising anti-inflammatory agent due to its ability to inhibit COX-2 expression. However, it remains largely unknown whether curcumin inhibits the UVB-induced COX-2 expression in HaCaT cells. This study was undertaken to clarify the effect of curcumin on the expression of COX-2 in UVB- irradiated HaCaT cells and further determined the molecular mechanisms associated with this process. In this study, we have found that the expression of COX-2 mRNA and protein were up-regulated in UVB-irradiated HaCaT cells in a dose- and time-dependent manner. Interestingly, treatment with curcumin strongly inhibited COX-2 mRNA and protein expressions in UVB-irradiated HaCaT cells. Notably, there was effective inhibition by curcumin on UVB-induced activations of p38 MAPK and JNK in HaCaT cells. The DNA binding activity of AP-1 transcription factor was also markedly decreased with curcumin treatment in UVB-irradiated HaCaT cells. These results collectively suggest that curcumin may inhibit COX- 2 expression by suppressing p38 MAPK and JNK activities in UVB-irradiated HaCaT cells. We propose that curcumin may be applied as an effective and novel sunscreen drug for the protection of photoinflammation.
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http://dx.doi.org/10.1038/emm.2005.25DOI Listing
June 2005